Talk:HIV

Edit request on 13 December 2011

To whomever it may concern,

I am a student in a Neuropsychology course at Boston University. My professor has previously contacted the administrators of this page to attain permission to add a section. We would truly appreciate if you would review and add the section we would like to contribute. Please let us know what changes are necessary.

Thank you so much.

Regarding illustration of the HIV

the illustration of the HIV

the nucleocapsid is not pointing to the capsid I think?

Please can someone clarify — Preceding unsigned comment added by 14.1.64.16 (talk • contribs) 08:51, 22 November 2012‎

Not sure what is being suggested. Do you have a reliable source that suggests a particular "correct" orientation of the nucleocapsid with respect to the capsid? -- Scray (talk) 18:16, 22 November 2012 (UTC)

Good article

I ask you to put the Good article tag in the Spanish edition. Thanks. --AAM-10 (talk) 18:48, 18 December 2012 (UTC)

You would need to go through the good article nomination process at Spanish Wikipedia rather than here. Doc James (talk · contribs · email) (if I write on your page reply on mine) 18:53, 18 December 2012 (UTC)

How does Human Immunodeficiency Virus (HIV) cause disease?

Getting started.

HIV virus entering the body meets the body’s scavenger cell - the macrophage.

HIV has two binding sites that fit with two binding sites on the macrophage to get inside

Once inside the macrophage the HIV enters its code into the macrophage’s DNA.

The macrophage is now under the control of HIV and makes an organelle (a factory within the cell) where new viruses are made.

The zombie macrophage makes a ‘viral synapse’ VS a binding site that allows the macrophage to bind onto other cells in a new way.

The VS gives the other cell a ‘kiss’ of HIV directly from the zombie macrophage to the other cell.

All this activity attracts the interest of T helper cells (Th) which come to investigate the macrophage.

T helper cells have both the CD4 receptor and each one has a unique receptor to detect a type of infection.

They detect the abnormal activity in the macrophage by ‘shaking hands’ with the Macrophage’s cell surface using CD4 protein and checking for presence of infection with their unique receptor.

The T helper cells (Th) with a receptor for HIV will tell the macrophages to self destruct (called TRAIL) and enlist other cells to kill the zombie macrophage if it does not comply.

HIV overrides the self destruct by telling the zombie macrophage to divide (using macrophage CSF).

If the zombie macrophage dies it destroys any cells in the area as it contains strong chemicals and releases many HIV particles.

If the zombie macrophage does not die it gives the T helper cell a ‘kiss’ of HIV as it shakes hands with them.

Once the interest in the infected macrophages dies down the zombie macrophage goes back to business as usual.

Macrophages have access to the most restricted areas such as the brain and shake hands with all the cells that have a CD4 receptor ( for instance perivascular microglial cells in the brain).

They leave in their wake infected cells that are used to make more HIV and then rupture releasing the HIV particles.

Progressive damage.

If all that HIV did was to create zombie macrophages then it is not likely that we would be aware of the virus.

The number of macrophages that become infected in HIV infected patients is kept low by the immune system until the latest stages of AIDS.

The T helper cells use their CD4 receptor to shake hands with macrophages and check that the macrophage has not encountered an infection that they have a receptor to.

The zombie macrophages are not detected by the T helper cells as they are looking for a different infection but they still give a kiss of HIV to each one.

The infected T helper cells self destruct or rupture releasing the viral particles which are dealt with by the immune system.

The damage to the immune system continues at a fairly constant rate as the number of macrophages that are infected, the number of interactions a macrophage makes and effectiveness of the rest of the immune system are similar in most people.

The number of T helper cells gradually declines until too few are left to detect infected cells.

Acquired Immunodeficiency syndrome AIDS.

AIDS is defined both by the absolute number of T Helper cells falling below 200 and the presence of certain types of infection.

As the T helper cells are best at detecting infection inside cells infections that live inside cells are the first to present.

Herpes viruses (shingles, CMV, Herpes simplex, Herpes virus 8 which causes Kaposi’s sarcoma), Toxoplasma and tuberculosis are all intracellular (live inside cells).

T helper cells are also good at controlling fungi so Pneumocystis and Candida start to spread. — Preceding unsigned comment added by 82.47.157.77 (talk) 11:49, 1 January 2013 (UTC)

physical property regulates HIV-1 infection

To whom may be concerned,

To fill the gap between HIV-1 "release" part to "entry to cells" part, HIV-1 undergoes a maturation process after budding out of infected cells. During this maturation process, HIV-1 protease cleaves its structural protein Gag into three small proteins, inducing a dramatic morphological change from a spherical particle containing a thick protein shell to a thin protein shell with a conical cone in the center. During this process, the stiffness of virion particle significantly reduces [1]. Recent study shows that the stiffness of HIV-1 virions can regulate its ability to enter the cells [2]. This novel regulatory level for HIV-1 replication may help prevent reentry of nascent virions into infected cells and facilitate the preservation of HIV-1 particles in extracellular environment.

References: 1. Kol N, Shi Y, Tsvitov M, Barlam D, Shneck RZ, Kay MS, Rousso I.A stiffness switch in human immunodeficiency virus.Biophys J. 2007 Mar 1;92(5):1777-83. 2. Pang HB, Hevroni L, Kol N, Eckert DM, Tsvitov M, Kay MS, Rousso I.Virion stiffness regulates immature HIV-1 entry. Retrovirology. 2013 Jan 10;10(1):4. — Preceding unsigned comment added by Zanticipate1028 (talk • contribs) 05:16, 19 January 2013 (UTC)

 Not done for now: Please say specifically where in the article you want this added. When you've done that, please reopen this request by changing the answered parameter to "no". You might also consider leaving a note at Wikipedia talk:WikiProject Medicine, asking someone there to review this request; deciding on its appropriateness involves several factors, and it's a bit above my pay grade. Rivertorch (talk) 08:44, 6 February 2013 (UTC)

Virion Maturation is already explained in the section "Replication cycle -> Assembly and release". I cleaned it up a bit and tried to make it more clear that maturation is essential for the virion to become infective. These new findings about physical stiffness do not seem important enough to me to be mentioned in the HIV article. --Xtothel (talk) 11:01, 28 February 2013 (UTC)

reasons for CD4+ T-cell decline

In the intro three reasons for CD4 decline are given without a reference. My understanding is that the current consensus is that non-specific immune activation is the main driving force for CD4 decline, whereas the three reasons stated are minor factors. http://www.ncbi.nlm.nih.gov/pubmed/23202514 I could look into this more when I get time. Maybe an immunologist can add some info. The original editor should add references. --Xtothel (talk) 10:37, 28 February 2013 (UTC)

Have changed the wording and added a ref Doc James (talk · contribs · email) (if I write on your page reply on mine) 16:25, 4 March 2013 (UTC)

Thanks! I have also added the ref from above now. --Xtothel (talk) 16:45, 4 March 2013 (UTC)

New diagram for viral entry - feedback requested

Hello,

I have recently made a new diagram about HIV entry into T-cells and I wish to include it in this article. Seeing as the HIV article is sorta high profile I wanted to ask for other's feedback and review of the figure before I go adding plastering it all over humanity's greatest repository of information, wikipedia that is.

This is the figure in question:

Artistically its a little bit busy. I got lazy with the inside of the virion, but if y'all think its necessary, I'll embellish it.

Scientifically, I don't see any glaring mistakes - but if I was 100% sure I wouldn't be asking. I tried to follow the general story that is told in our article. There are scads of similar diagrams around the ol'net that all hit the same points, so i don't think there should be any huge paradigm shifts in my presentation here.

I haven't written the figure legend for it yet, but I'll follow the article. The red arrows try to highlight the important spots of each step.

Adenosine^talk 01:21, 12 March 2013 (UTC)

Hey Adenosine, very nice work! I always wondered why there was no entry diagram with actual crystal structure data, and yours looks really good. However I think it is more interesting for experts and a bit too busy and un-scalable for the wikipedia page. But I know nothing good exists, yet. I think a line drawing would be more suited but don't have the time/skills. Something like in here (but of course it's copyrighted) without the shading would be nice: http://www.ncbi.nlm.nih.gov/pubmed/15102550. Xtothel (talk) 10:23, 14 March 2013 (UTC)

oh and, yes, scientifically it looks good although the reason people usually do not use the crsytal structures is probably that that implies more precise knowledge than we actually have. These structures are of monomeric, heavily truncated proteins. The way they are oriented in the viral spike assembly is unknown. So drawings like that should always point out that caveat in the legend. Xtothel (talk) 10:36, 14 March 2013 (UTC)

I really like the figure - and I do think it scales well (from the Commons page even the 500px version looks good, and it nicely switches the font to sans serif and key features are still visible). A few comments:

• showing a mature capsid seems important, given the role of protease inhibitors in antiretroviral therapy
• I had the impression that CD4 binding of gp120 induced a conformational change that exposed an otherwise occluded face to which the chemokine receptor binds. The way the figure is drawn, it looks like an already-exposed loop just becomes more accessible. If I'm not clear, I can try to find an example
• The figure is of such high quality that I have to ask - is this based on a figure we should look at, to ensure there are no infringement issues? I say this in praise - it's really gorgeous - but you provide so few details about sourcing and drawing tools that one is left wondering. I hope it really is free-and-clear, because I'd love to see it included in the article. Elements could be re-used in other ways.
• Shouldn't "CCR5" be all-caps?

Nice work - thanks for your contribution. -- Scray (talk) 11:07, 14 March 2013 (UTC)

Xtothel, I actually used that article as a reference for the general layout. I could try to simplify it a bit - but I want to get across that behind the balls and cylinders that predominate other pictures there's actual discrete structure that we know a lot about. But maybe there's away of making it all less busy without losing the detail and depth. I have added the interior of the virion in my next version. Scray, I certainly don't think I infringed on anything, though I'm no lawyer, I can (and will) add citations from my sources. Everything was drawn from scratch. I used publicly available protein structure data to drawn gp120, i'll happily cite it if need be. The general design was inspired by the figure in the paper that Xtothel mentioned. - - Adenosine^talk 00:30, 19 March 2013 (UTC)